: Preterm labor and birth is responsible for 75 percent of all infant mortalities. Treatments to prevent premature birth could have a profound effect on fetal mortality and morbidity. Cervical ripening precedes the onset of normal labor and can lead to preterm labor if the cervix dilates early. NO, which is produced by NO synthase enzymes (NOS), is believed to play a role in cervical ripening and dilation. Endogenous release of PGs produced by cyclooxygenase (COX) enzymes is also thought to play a role in cervical ripening. The objective of the research is to characterize COX and NOS activity, as well as NO and PG production in the cervix as they relate to cervical ripening. The interactions between the two systems will also be investigated. Aim one is to demonstrate if there is a temporal relationship between COX and NOS under normal and LPS treated conditions by characterizing the patterns of expression and cellular distribution of COX and NOS during pregnancy, labor, and postpartum in rat cervical tissue. Aim two examines whether exogenous (NO-donors) and endogenous NO (LPS) effects COX expression in the absence and presence of NOS inhibitors by determining the patterns of expression and cellular distribution of COX during pregnancy, labor, and postpartum in rat cervical tissue. Aim three estimates if the activation of metabolites of the COX pathway or the exogenous treatments of PGs effect NOS expression in the absence or presence of COX inhibitors by determining the patterns of expression and cellular distribution of NOS during pregnancy, labor, and postpartum in rat cervical tissue.